The general objective of this project is to determine the possible immunologic basis for the enhanced susceptibility of the diabetic host to such an opportunistic fungus infection as candidiasis. Herein, possible changes in cell-mediated immunity in the diabetic mouse will be investigated. In this category are production of lymphokines in vivo, extent of activity suppressor cells, behavior of T and B lymphocytes, and behavior of macrophages. Also, the basis of the conversion from the yeastlike to hyphal phase of Candida albicas and the associated increase in pathogenicity will be investigated. Attempts to increase the resistance to these agents will be made by passive administration of lymphokine-containing serum and of purified fractions therefrom to infected hosts. These studies should therefore provide important information toward the understanding as to why insulin-deficient (alloxan-induced) and insulin-resistant (genetically-determined) diabetic mice are immunologically deficient and therefore susceptible to certan infections, such as those caused by C. albicans.